Evidence map›Paper›PMID 31783925›Full record

ArticleBiological research2019

Long non-coding RNA MALAT1 enhances the apoptosis of cardiomyocytes through autophagy inhibition by regulating TSC2-mTOR signaling.

Hao Hu, Jiawei Wu, Xiaofan Yu, Junling Zhou, Hua Yu, Likun Ma

Open access · goldAbstract read
In one paragraph

Article in Biological research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.1field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Programmed cardiomyocyte death in myocardial infarction.Apoptosis : an international journal on programmed cell death · 2025
    Review
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  5. Review
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  19. Article
  20. Regulation of Pyroptosis by ncRNA: A Novel Research Direction.Frontiers in cell and developmental biology · 2022
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Hao HuDepartment of Cardiovascular, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, No. 1 Swan Lake Road, Hefei, 230001, Anhui, People's Republic of China.
Jiawei WuDepartment of Cardiovascular, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, No. 1 Swan Lake Road, Hefei, 230001, Anhui, People's Republic of China.
Xiaofan YuDepartment of Cardiovascular, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, No. 1 Swan Lake Road, Hefei, 230001, Anhui, People's Republic of China.
Junling ZhouDepartment of Cardiovascular, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, No. 1 Swan Lake Road, Hefei, 230001, Anhui, People's Republic of China.
Hua YuDepartment of Cardiovascular, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, No. 1 Swan Lake Road, Hefei, 230001, Anhui, People's Republic of China.
Likun MaDepartment of Cardiovascular, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, No. 1 Swan Lake Road, Hefei, 230001, Anhui, People's Republic of China. likunma633@yeah.net.
University of Science and Technology of China · CN

Funding

National Natural Science Foundation of China No. 81870192
6 · The paper itself

Abstract

backgroundOur previous study showed that knockdown of long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) attenuated myocardial apoptosis in mouse acute myocardial infarction (AMI). This study aims to explore whether MALAT1 enhanced cardiomyocyte apoptosis via autophagy regulation and the underlying mechanisms of MALAT1 regulating autophagy.

methodsCardiomyocytes were isolated from neonatal mice and then stimulated with hypoxia/reoxygenation (H/R) injury to mimic AMI. The autophagy level was assessed using GFP-LC3 immunofluorescence and western blot analysis of autophagy-related proteins. RNA pull-down and RNA immunoprecipitation (RIP) was performed to analyze the binding of MALAT1 and EZH2. Chromatin immunoprecipitation (ChIP) assay was performed to analyze the binding of TSC2 promoter and EZH2. The cell apoptosis was evaluated using TUNEL staining and western blot analysis of apoptosis-related proteins.

resultsH/R injury increased MALAT1 expression in cardiomyocytes. Furthermore, MALAT1 overexpression inhibited, whereas MALAT1 knockdown enhanced the autophagy of cardiomyocytes. Moreover, MALAT1 overexpression recruited EZH2 to TSC2 promoter regions to elevate H3K27me3 and epigenetically inhibited TSC2 transcription. Importantly, TSC2 overexpression suppressed mTOR signaling and then activated the autophagy. Further results showed that MALAT1 inhibited proliferation and enhanced apoptosis of cardiomyocytes through inhibiting TSC2 and autophagy.

conclusionThese findings demonstrate that the increased MALAT1 expression induced by H/R injury enhances cardiomyocyte apoptosis through autophagy inhibition by regulating TSC2-mTOR signaling.

Indexed as

AnimalsApoptosisAutophagyBlotting, WesternChromatin ImmunoprecipitationFluorescent Antibody TechniqueMiceMyocytes, CardiacReverse Transcriptase Polymerase Chain ReactionRNA, Long NoncodingSignal TransductionTOR Serine-Threonine KinasesTuberous Sclerosis Complex 2 ProteinRNA, Long NoncodingTOR Serine-Threonine KinasesTSC2 protein, humanTuberous Sclerosis Complex 2 ProteinAutophagyCardiomyocyte apoptosisEZH2MALAT1TSC2-mTOR

Identifiers

PMID31783925
PMCPMC6883637
OpenAlexW2989679864

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.